Fig. 4: Oncogenic KRAS significantly suppressed type I IFNs via DNMT3b-mediated STING methylation.

A Dot plot heatmaps showing DNA methylation levels in the STING promoter in CCLE (red = hypermethylation). The location of each position is as follows: P1, 5:138861649; P2, 5:138861807 and P3, 5:138862442. One-way ANOVA t test. ***p < 0.001. B The DNA methylation levels in the TMEM173(STING) promoter was evaluated in the post-neoCRT surgical tissues. P1, 5:138861649 and P2, 5:138861807. C The relationship between STING promoter P1/P2-1 methylation and KRAS mutations (G12/G13 mutations) was evaluated by Pyrosequencing. One-way ANOVA t test. *p < 0.05. D The relationship between STING promoter P2-2-1/P2-2-2 methylation and KRAS mutations (G12/G13 mutations) was evaluated by Pyrosequencing. One-way ANOVA t test. E The level of tumor STING in KRAS^WT pair-matched pre-neoCRT biopsies and post-neoCRT surgical tissues. F The level of tumor STING after neoCRT treatment was evaluated in KRAS^WT-CRC patients (p = 0.03, n = 42). One-way ANOVA t test. G The level of tumor STING in KRAS^Mut pair-matched pre-neoCRT biopsies and post-neoCRT surgical tissues. The level of tumor STING after neoCRT treatment was evaluated in KRAS^Mut-CRC patients (p = 0.15, n = 17). One-way ANOVA t test. H KM analysis on tumor STING in KRAS^WT-CRC patients (p = 0.0366, n = 41). Log-rank p test.